目的:探讨脑血管造影的3 D打印技术在颅内动脉瘤患者开颅夹闭术治疗中的应用效果.方法:选择2020年1月至2022年12月我院收治的70例颅内动脉瘤患者采用随机数字表法分为观察组与对照组,各35例.对照组应用传统开颅夹闭术治疗,观察组基于脑血管造影的3D打印技术辅助开颅夹闭术治疗.比较两组手术相关评价指标水平;比较两组围术期各时间点血流动力学指标水平变化情况;比较两组围术期各类并发症发生风险.结果:观察组术前准备时间、术中操作时间与住院时间均短于对照组(P<0.05).两组T0～T3时间点ICP、MAP与HR均呈现明显升高趋势(F=17.640,36.310;P<0.05);观察组T1～T3时间点ICP、MAP与HR均明显低于对照组(P<0.05).观察组围术期并发症总发生率为0.00％,低于对照组的14.29％(P<0.05).结论:脑血管造影的3D打印技术在颅内动脉瘤开颅夹闭术治疗患者中的应用效果较好,可缩短患者手术治疗时间与术后康复时间,且对其术中血流动力学影响程度较小,患者围术期并发症风险较低,值得推广应用.

Abstract Background: The expression and role of the endothelin converting Enzyme like1 (ECEL1) gene in hepatocellular carcinoma（HCC）was unclear. The purpose of this study was to understand the expression of ECEL1 in HCC tissues and cells and its effects on the proliferation and apoptosis of HCC cells, so as to provide a new therapeutic target for the prevention and treatment of HCC. Methods: (1) The expression of ECEL1 between HCC and normal liver tissues was analyzed by TCGA database, and the analysis results of TCGA database were verified by immunohistochemical staining. The correlation between the expression of ECEL1 and the survival time of HCC patients was analyzed by Kaplan Meier plotter database. (2) On the basis of confirming that HCC cell lines could express ECEL 1 gene, ECEL 1 expression in HCC cells were silenced by lentivirus-mediated RNAi technology, and observed the functional changes in the direction of proliferation of HCC cells by clone formation, Celigo count, MTT, etc. At the same time, the functional changes of apoptosis direction of HCC cells were observed, such as apoptosis, Caspase-3/7 activity, after silencing ECEL1. The HCC cells that RNAi effectively silenced ECEL1 were injected subcutaneously into nude mice to observe the ability of ECEL1 to regulate the proliferation of liver cancer in vivo. (3) The expression profile microarray was used to detect the differential expression of the downstream genes after ECEL1 silencing in HCC cells, and quantitative real-time PCR（qRT-PCR）and Western Blot were applied to verify some genes related to HCC proliferation and apoptosis to explore the possible mechanism of ECEL1 regulating the proliferation and apoptosis of hepatocellular carcinoma. Results: (1) The original data of 374 RNAseq samples (Cancer/Normal) in TCGA database were filtered, standardized, BCV (biological coefficient of variation) quality controlled and statistical analyzed. It showed that the expression level of ECEL1 in HCC tissues were higher than that in normal liver tissue (p<0.05). The results of immunohistochemical staining showed that there were significant differences in the expression of ECEL1 gene between liver cancer tissues and normal liver tissues, which were consistent with the analysis results of TCGA database. (2) The expression of ECEL1 gene in various HCC cell lines were detected by qRT-PCR, and the results using GAPDH as an internal reference showed that ECEL1 gene was expressed in various HCC cells. (3) Clone formation, Celigo and MTT assay showed that the proliferation of BEL-7404 and Huh-7 cells were significantly inhibited after ECEL1 silencing (p<0.05).(4) Flow cytometry showed that the apoptosis rate of BEL-7404 and Huh-7 cells increased significantly after ECEL1 silencing (P<0.01). After ECEL1 silencing, BEL-7404 cells in S phase decreased significantly, while those in G2/M phase increased significantly (P<0.01). (5)Caspase-Glo®3/7 Assay kit showed that the activity of Caspase-3/7 in BEL7404 and Huh-7 cells were significantly increased after silencing the ECEL1 gene (P<0.01). (6) The results of animal tumorigenesis experiment showed that the tumor volume of shECEL1 group was smaller than that of shCtrl group, the tumor weight was lighter, the total fluorescence expression in the tumor area and the average fluorescence expression per cm2in the region were weaker. (7) The expression profile chip detection showed that 371 genes were up-regulated and 377 genes were down regulated in the shECEL1 group. Bioinformatics analysis, qRT-PCR and Western Blot verification showed that the expression of DUSP1, THBS1 and PTEN was up-regulated, while the expression of EGR1 was down regulated. Conclusions: The ECEL1 was highly expressed in liver cancer tissues and ECEL1 gene was significantly related to survival time of patients with liver cancer;The silencing ECEL1 expression in liver cancer cells could induce cell apoptosis, inhibit cell proliferation and the growth of subcutaneous transplanted tumors; The expression of DUSP1, THBS1, PTEN may participate in the inhibition of liver cancer cell proliferation. These results indicate that ECEL 1 gene is a gene related to the proliferation and apoptosis of hepatoma cells

目的 基于哺乳动物雷帕霉素靶蛋白(mTOR)/p70 核糖体S6 蛋白激酶(P70S6K)通路研究上调微小核糖核酸(miR)-205-5p对肝癌细胞增殖、侵袭的影响.方法 肝癌HepG2 细胞株经过细胞培养、转染后,分为上调miR-205-5p组、肝癌组和阴性对照组.实时荧光定量(RT)-聚合酶链反应(PCR)检测miR-205-5p表达,观察肝癌细胞增殖、凋亡、侵袭能力,Western印迹检测p-mTOR、p-P70S6K、mTOR、P70S6K蛋白表达.结果 上调miR-205-5p组miR-205-5p表达显著高于肝癌组和阴性对照组,阴性对照组显著高于肝癌组(均P＜0.05).在24、48、72 h,上调miR-205-5p组细胞光密度值均显著低于阴性对照组和肝癌组,阴性对照组光密度值均显著低于肝癌组,在72h差异表现最为明显(P＜0.05),阴性对照组和肝癌组随着时间延长,光密度值逐渐显著升高,上调miR-205-5p组光密度值逐渐显著降低(均P＜0.05).上调miR-205-5p组72h细胞增殖数、细胞侵袭数显著低于肝癌组和阴性对照组,细胞凋亡数显著高于肝癌组和阴性对照组(均P＜0.05).上调miR-205-5p组mTOR、P70S6K、p-mTOR、p-P70S6K蛋白表达显著低于肝癌组和阴性对照组(均P＜0.05).结论 上调miR-205-5p可以影响mTOR/P70S6K信号通路的活性,参与肝癌细胞侵袭、增殖、凋亡的过程.

目的 观察神经内镜辅助下血肿清除术与软通道穿刺引流术治疗高血压脑出血的疗效.方法 60例高血压脑出血患者,以随机数字表法分成研究组与对照组,各30例.研究组接受神经内镜辅助下血肿清除术治疗,对照组接受软通道穿刺引流术治疗.比较两组围手术期指标,术前、出院前的相关评分(神经功能缺损、日常生活能力、昏迷指数评分)及血肿量.结果 研究组手术时间(72.75±8.52)min、住院时间(12.25±1.93)d短于对照组的(110.49±23.45)min、(17.61±2.72)d,术中出血量(74.55±14.43)ml少于对照组的(181.37±29.51)ml,差异有统计学意义(P<0.05).出院前,两组神经功能缺损评分、血肿量低于术前,且研究组神经功能缺损评分(10.98±2.18)分、血肿量(3.55±0.61)ml低于对照组的(15.02±3.12)分、(7.72±1.17)ml;两组日常生活能力评分、昏迷指数评分高于术前,且研究组日常生活能力评分(84.80±7.77)分、昏迷指数评分(13.88±0.30)分高于对照组的(79.30±6.05)、(12.06±0.35)分,差异均有统计学意义(P<0.05).研究组术后并发症发生率3.33％低于对照组的26.67％,差异有统计学意义(P<0.05).结论 给予高血压脑出血患者神经内镜辅助下血肿清除术治疗,可显著的缩短患者的手术与住院时间,减少术中出血量,改善术后患者的日常生活能力、昏迷状态,减轻神经功能缺损程度,降低脑部血肿量,减少术后并发症的发生,效果理想.

目的 探讨破裂前交通动脉瘤急性期行血管内介入栓塞治疗的疗效.方法 回顾性分析我科采用急性期介入栓塞治疗的38例破裂前交通动脉动脉瘤的临床资料.结果 38例中,26例应用支架辅助弹簧圈栓塞,12例单纯弹簧圈栓塞,术后即刻造影显示,Roymond分级Ⅰ级29例,Ⅱ级6例,Ⅲ级3例,无手术例死亡病例.出院时mRS评分:0分24例,1分6例,2分3例,3分2例,4分1例,5分2例.结论 急性期介入栓塞治疗破裂前通动脉瘤是安全有效的.

Major histocompatibility complex, class II, DQ beta 1 antisense RNA 1 (HLA-DQB1-AS1) conferred the susceptibility to hepatocellular carcinoma. Sustaining cell growth and resisting apoptosis are two hallmarks of hepatocellular carcinoma. The present study explored the role of HLA-DQB1-AS1 in the proliferation and apoptosis of hepatocellular carcinoma cells and investigated its downstream pathway. Colony formation assay was performed to assess cell proliferation. Cell apoptosis was assessed with the TdT-mediated dUTP nick end labeling method. HLA-DQB1-AS1 deficiency exerts antiproliferative and proapoptotic effects on hepatocellular carcinoma cells. Moreover, based on bioinformatic analysis combined with the results of RNA immunoprecipitation assay, HLA-DQB1-AS1 was revealed to bind with zinc finger RANBP2-type containing 2 (ZRANB2) protein. ZRANB2 was upregulated in hepatocellular carcinoma at a clinical and cellular level. HLA-DQB1-AS1 caused no significant effects on ZRANB2 mRNA and protein expression. ZRANB2 knockdown suppressed cell proliferation and enhanced cell apoptosis of hepatocellular carcinoma. Moreover, ZRANB2 overexpression rescued the anticancer effect of silenced HLA-DQB1-AS1 in hepatocellular carcinoma cells. In conclusion, HLA-DQB1-AS1 promotes cell proliferation and inhibits apoptosis in hepatocellular carcinoma by the interaction with ZRANB2 protein.

Emerging evidence has uncovered that noncoding RNAs (ncRNAs) contribute to the development of hepatocellular carcinoma (HCC). Nevertheless, the functions of the majority of long ncRNAs (lncRNAs) in HCC are unknown. Here, we intend to probe the function of lncRNA NUTM2A-AS1 in the evolvement of HCC and the related mechanism. Expression levels of lncRNA NUTM2A-AS1, miR-186-5p and KLF7 mRNA in HCC tissues and adjacent non-tumor tissues were monitored. Gain- or loss-of-function assays were utilized to investigate the biological functions of lncRNA NUTM2A-AS1, miR-186-5p and KLF7 in HCC cell lines (including HCCLM3 and Huh7). Western blot was implemented for the detection of the epithelial–mesenchymal transition (EMT)-related proteins (including E-cadherin, Vimentin and Snail), KLF7, Wnt, β-catenin, and stemness-related proteins (Nanog, OCT4, YKL40, and CD133). Furthermore, the targeted associations between lncRNA NUTM2A-AS1, miR-186-5p, and KLF7 were verified by bioinformatics analysis, dual-luciferase reporter and RNA immunoprecipitation (RIP) assays. As a result, lncRNA NUTM2A-AS1 and KLF7 profiles were heightened in the HCC tissues versus adjacent normal tissues, while miR-186-5p had the opposite expression tendency. Up-regulation of lncRNA NUTM2A-AS1 was related to tumor size, advanced tumor stage, and lymph node metastasis of HCC patients. Functionally, overexpression of lncRNA NUTM2A-AS1 heightened HCC cells’ growth, invasion, EMT, and stemness and repressed their apoptosis by activating the Wnt/β-catenin pathway. In contrast, up-regulation of miR-186-5p or inhibition of KLF7 had reverse effects. In vivo, lncRNA NUTM2A-AS1 overexpression facilitated tumor growth and EMT, accompanied by declined miR-186-5p levels and enhanced KLF7 expression. The mechanistic studies revealed that miR-186-5p served as a common target of lncRNA NUTM2A-AS1 and KLF7. As hinted by the rescue experiments, NUTM2A-AS1 partly abated miR-186-5p-mediated anti-tumor effects in HCC cells, whereas KLF7 knockdown reversed the promotive effects of NUTM2A-AS1. LncRNA NUTM2A-AS1 accelerated the evolution of HCC by up-regulating the KLF7/Wnt/beta-catenin pathway through sponging miR-186-5p.

OBJECTIVE:To explore the value of serum activin A (ACT-A) level in early identification of moderate and severe acute pancreatitis (AP). METHODS:A prospective case control study was conducted. A total of 120 patients with AP admitted to department of hepatobiliary surgery of Affiliated Nanhua Hospital of Hengyang Medical College of University of South China between October 2020 and April 2022 were recruited. According to the revised Atlanta classification, all patients were classified into mild AP group and moderate-to-severe AP group. The blood samples within 24 hours of onset were drawn, and the serum ACT-A and C-reactive protein (CRP) levels were detected by enzyme-linked immunosorbent assay (ELISA). The Ranson score and the modified CT severity index (MCTSI) were performed. Pearson correlation method was used to analyze the correlation of various parameters. The receiver operator characteristic curve (ROC curve) was plotted to analyze the predictive value of ACT-A and CRP for moderate-to-severe AP. RESULTS:A total of 120 patients with AP were enrolled, including 83 patients with mild AP and 37 patients with moderate-to-severe AP. Serum ACT-A and CRP levels within 24 hours of onset in the moderate-to-severe AP group were significantly higher than those in the mild AP group [ACT-A (ng/L): 140.4±37.7 vs. 53.9±30.5, lg CRP: 1.42±0.91 vs. 0.77±0.70, both P < 0.01], and the Ranson score and MCTSI score were also significantly higher than those in the mild AP group (Ranson score: 5.3±1.3 vs. 1.8±1.6, MCTSI score: 5.5±1.0 vs. 2.7±1.2, both P < 0.01). Correlation analysis showed that the serum ACT-A level was positively correlated with serum CRP level, Ranson score and MCTSI score (R2 value was 0.272, 0.841, 0.616, respectively, all P < 0.05). ROC curve analysis showed that the serum ACT-A, CRP and Ranson score had predictive value for moderate-to-severe AP. The area under the ROC curve (AUC) was 0.948 [95% confidence interval (95%CI) was 0.909-0.986], 0.711 (95%CI was 0.606-0.815), 0.946 (95%CI was 0.910-0.982), respectively. When serum ACT-A > 112.6 ng/L, the sensitivity and specificity of predicting moderate-to-severe AP were 78.38% and 96.39%, respectively, which was better than serum CRP with sensitivity and specificity of 72.92% and 66.27%, respectively, and the specificity was better than Ranson score (71.08%). CONCLUSIONS:ACT-A can be detected in the early stage of AP, and it is positively correlated with the disease severity, which can early identify moderate-to-severe AP.

Background: To investigate the clinical effects of intubation and sphincterotomy with wire-guided incision knife plus balloon dilatation (ISBD) in the treatment of choledocholithiasis, a randomized controlled trial was conducted. Methods: A total of 270 patients with choledocholithiasis confirmed by computed tomography or magnetic resonance imaging from January 2016 to July 2018 in our hospital were enrolled in the research. All patients were randomly divided into 3 groups: ISBD group, endoscopic sphincterotomy (EST) group, and endoscopic sphincterotomy plus balloon dilation group, respectively. The clinical effects, complications, and inflammation indexes of the 3 groups were detected. SPSS software was used for statistics and analysis of results. Results: There were no significant differences in basic characteristics of the 3 groups. Although there was no significant difference in the total stone clearance rate among the 3 groups, the first stone clearance rate and the large stone clearance rate in ISBD group were significantly higher than those in EST group. Compared with the other 2 groups, the total operation time and complications in ISBD group were significant lower. The serum levels of interleukin-6, C-reactive protein (CRP), procalcitonin (PCT), carbohydrate antigen 19-9, and carcinoembryonic antigen in ISBD group were significant lower than those in EST group, and CRP and PCT in ISBD group were markedly lower than those in endoscopic sphincterotomy plus balloon dilation group. Conclusions: ISBD treatment simplifies the operation procedure, shortens the operation time, reduces postoperative inflammation and complications, and makes ERCP stone removal simpler, safer, and more efficient for patients with common bile duct stones.

BACKGROUND AND AIMS:Androgen receptor (AR) has been reported to play an important role in the development and progression of man's prostate cancer. Hepatocellular carcinoma (HCC) is also male-dominant, but the role of AR in HCC remains poorly understood. Mechanistic target of rapamycin complex 1 (mTORC1) also has been reported to be highly activated in HCC. In this study, we aimed to explore the role of AR phosphorylation and its relationship with mTORC1 in hepatocarcinogenesis. APPROACH AND RESULTS:In vitro experiment, we observed that mTORC1 interacts with hepatic AR and phosphorylates it at S96 in response to nutrient and mitogenic stimuli in HCC cells. S96 phosphorylation promotes the stability, nuclear localization, and transcriptional activity of AR, which enhances de novo lipogenesis and proliferation in hepatocytes and induces liver steatosis and hepatocarcinogenesis in mice independently and cooperatively with androgen. Furthermore, high ARS96 phosphorylation is observed in human liver steatotic and HCC tissues and is associated with overall survival and disease-free survival, which has been proven as an independent survival predictor for patients with HCC. CONCLUSIONS:AR S96 phosphorylation by mTORC1 drives liver steatosis and HCC development and progression independently and cooperatively with androgen, which not only explains why HCC is man-biased but also provides a target molecule for prevention and treatment of HCC and a potential survival predictor in patients with HCC.

ObjectiveTo obtain HSC-T6 cells with stable expression of Cas9 protein and HSC-T6-COX-2-/- cells with COX-2 gene defect by transfecting HSC-T6 cells with CRISPR/Cas9 lentiviral vector, and to provide a good method for further functional research and new strategies for the clinical treatment of liver fibrosis. MethodsThe COX-2 gene-specific sgRNAs (COX-2-sgRNA-1, COX-2-sgRNA-2, COX-2-sgRNA-3) were designed, synthesized, and connected to the GV371 vector, and the recombinant plasmid and the packaging plasmid were transfected into 293T cells to form lentivirus particles; the fluorescence method was used to measure virus titer. The most appropriate amount of the virus was calculated based on MOI. Lenti-Cas9-puro was transfected into HSC-T6 cells, and HSC-T6-Cas9 cells were screened out by puromycin; Lenti-COX-2-sgRNA-EGFP was transfected into HSC-T6-Cas9 cells to obtain HSC-T6-COX-2-/- cells. Cruiser enzyme digestion and Western blot were used to verify gene knockout at the gene and protein levels. An analysis of variance was used for comparison of continuous data between multiple groups, and the least significant difference t-test was used for further comparison between two groups. ResultsSequencing verified that the COX-2-sgRNA expression vector was constructed successfully. Recombinant expression plasmids and packaging plasmids were transfected into 293T cells to form lentivirus particles, and the fluorescence method showed a virus titer of ＞1×108. HSC-T6 cells with stable expression of Cas9 protein and HSC-T6-COX-2-/- cells with COX-2 gene defect were successfully constructed. The HSC-T6-Cas9 group had significantly higher relative mRNA expression of LV-Cas9-Puro than the CON group (541.93±105.76 vs 1.00±0.02, t=12.995, P＜0.01). Cruiser enzyme digestion and Western blot showed that the CRISPR/Cas9 lentivirus expression vectors played a role in the target, among which COX-2-sgRNA-2 knockout had the most significant effect, and this group had a significant reduction in the protein expression level of COX-2 compared with the CON group and the NC group (both P＜0.05), suggesting that COX-2-sgRNA was active. ConclusionA CRISPR/Cas9 lentivirus vector is successfully constructed for COX-2 target gene, and HSC-T6-COX-2-/- cells with stable COX-2 gene knockout are obtained.

目的 探讨骨髓间充质干细胞(bone marrow mesenchymal stem cells,BMSCs)移植对大鼠结直肠组织放射性损伤的修复作用及其可能机制.方法 36只健康SD大鼠,随机分为空白对照组、γ射线照射组、BMSCs治疗组.γ射线照射组及BMSCs治疗组予12Gy的60Coγ 射线一次性全腹照射,BMSCs治疗组照射后第2d尾静脉注射大鼠骨髓间充质干细胞注射液1ml(1×106个/ml).3组大鼠均于实验第7d经心脏采血后处死并留取结直肠标本,采用HE染色法观察黏膜组织病理形态变化;TUNEL法检测黏膜细胞的凋亡情况;ELISA法测定外周血TNF-α和IL-10含量.结果 HE染色示γ射线照射组大鼠结直肠肠黏膜形态和结构发生明显病理损伤改变;BMSCs治疗组较γ 射线照射组病理受损程度减轻.γ 射线照射组大鼠结直肠肠黏膜细胞凋亡率较空白对照组显著升高,BMSCs治疗组则显著低于γ射线照射组.γ射线照射组大鼠外周血中TNF-α含量较空白对照组显著升高,IL-10升高无统计学差异;BMSCs治疗组TNF-α低于γ射线照射,IL-10含量显著高于γ射线照射组.结论 BMSCs移植可减轻结直肠粘膜的放射性病理性损伤,并可通过抑制细胞凋亡减轻大鼠放射性结直肠损伤,通过抑制炎症反应减轻大鼠放射性结直肠损伤.

ObjectiveTo investigate the effect and significance of cyclooxygenase-2 (COX-2) inhibitors on the expression of the Acsl gene family in the ileum of rats with nonalcoholic fatty liver disease (NAFLD). MethodsA total of 45 Sprague-Dawley rats were randomly divided into normal control group (15 rats given normal diet), NAFLD model group (15 rats given high-fat diet), and nimesulide group (15 rats given high-fat diet and nimesulide). All rats were sacrificed after 12 weeks of feeding, and then blood samples were collected from the inferior vena cava to measure total cholesterol (TC) and triglyceride (TG). HE staining and oil red O staining were performed for the liver to evaluate the degree of hepatic steatosis in each group, and quantitative real-time PCR was used to measure the mRNA expression of the Acsl family genes in the ileum. An analysis of variance was used for comparison of continuous data between multiple groups, and the least significant difference t-test was used for further comparison between two groups. ResultsCompared with the normal control group, the NAFLD model group had significant increases in serum TC and TG and marked hepatic steatosis (all P＜0.05); compared with the NAFLD model group, the nimesulide group had significant reductions in serum TC and TG and degree of hepatic steatosis (all P＜0.05). Compared with the normal control group, the NAFLD model group had a significant increase in the expression of COX-2 in the ileum (P＜0.05), and compared with the NAFLD model group, the nimesulide group had a significant reduction in the expression of COX-2 in the ileum (P＜005). Compared with the normal control group, the NAFLD model group had significant increases in the mRNA expression of Acsl3 and Acsl5 in the ileum (both P＜0.05), and compared with the NAFLD model group, the nimesulide group had significant reductions in the mRNA expression of Acsl3 and Acsl5 (both P＜0.05). ConclusionThe COX-2 inhibitor nimesulide can regulate the expression of the Acsl gene family in the ileum of rats with NAFLD, suggesting that COX-2 inhibitors may inhibit the progression of NAFLD through the Acsl gene.

Acute lung injury is characterized by alveolar vascular barrier injury, and protein-rich pulmonary oedema. Alveolar fluid clearance is closely related to the prognosis of patients with acute lung injury. Melatonin has been shown to have a protective effect on multiple organ injury induced by sepsis. In this study we investigated the effect of melatonin on alveolar fluid clearance (AFC) and explored its potential mechanisms in sepsis-induced acute lung injury. The cecal ligation and puncture was adopted to establish mouse sepsis model. Morphological changes of lung tissues with the hematoxylin staining were observed. AFC and lung wet/dry weight ratio were measured to assess pulmonary edema. Inflammatory mediators in bronchoalveolar lavage fluid were analyzed via enzyme-linked immunosorbent assay. NAD+/NADH and SIRT1 activity were measured by colorimetric assay kit. The protein expressions of epithelial sodium channel (ENaC), silent information regulator1 (SIRT1), SGK1 and Nedd4-2 were immunoblotted by western blot in vivo and in vitro. The distribution of α-ENaC and SIRT1 was detected by immunofluorescence. We found that melatonin attenuated sepsis induced lung injury, improved survival rate, enhanced alveolar fluid clearance, improved SIRT1 activity, increased protein expressions of SIRT1 and ENaC, and activated SGK1/Nedd4-2 pathway. Furthermore, SIRT1 inhibitor EX527 counteracted the effects of melatonin on alveolar fluid clearance and ENaC. These results revealed that melatonin enhanced ENaC-mediated AFC via the SIRT1/SGK1/Nedd4-2 signaling pathway. Our study demonstrated that melatonin might provide a novel therapeutic strategy for sepsis-induced acute lung injury.

Objective To study the radiation-induced mitochondrial damage and energy metabolic alteration in pancreatic exocrine cells,and to explore underlying mechanism.Methods Rat pancreatic exocrine cells (AR42 J) were divided into control group and experimental group irradiated with 6 Gy of X-rays.Mitochondrial membrane potential was detected at 24,48,72 and 96 h,the lactic acid and ATP production were detected at 24 h and 48 h,and reactive oxygen species (ROS) were detected at 24 h after irradiation.The expressions of energy metabolism related factors of HIF-1α,LDHA and PDH were detected by Western blot.The animal experiments were conducted to confirm the changes.According to random number table,eight rats were randomly divided into two groups with 4 rats in each.The irradiated group was exposed to 12 Gy of X-rays,while the control group sham-irradiated.Results Compared with the nonirradiated control group,the mitochondrial membrane potential (△Ψm) of the experimental group was progressively decreased at 24-96 h after irradiation (t =5.438-17.687,P＜0.05).The ATP content in the experimental group decreased at 24 h and 48 h (q=17.300,8.328,P＜0.05),the lactic acid increased (q =21.790,16.250,P＜0.05),and the ROS level increased (t =7.935,P＜0.05).The expressions of HIF-1α and LDHA were significantly increased,but PDH was reduced after radiation.Silencing HIF-1α by siRNA eliminated radiation-induced energy metabolic alteration.These changes were confirmed with animal experiments by locally irradiating rats.Conclusions The expression of HIF-1α is upregulated by irradiation,which leads to the change of energy metabolism as the enhancement of glycolysis pathway and the inhibition of aerobic oxidation of mitochondria in pancreatic exocrine cells.

选择GDM患者100例,给予运动、饮食等干预,分为依从性良好组(A组)52例,和依从性差组(B组)48例.结果 干预后,A组FBG、2hPG、HbA1c等改善情况优于B组(P＜0.05);在早产、先天子痫等妊娠结局方面比较,A组发生率均低于对照组,自然分娩率高于B组(P＜0.05);妊娠期高血压综合征、产褥感染及妊娠期并发症的总发生率均显著低于B组(P＜0.05);巨大儿、低出生体重儿、新生儿低血糖和新生儿窘迫,及不良围产儿的总发生率均显著低于B组(P＜0.05).结论 GDM患者良好的生活方式干预依从性有助于其控制血糖,并进一步改善母婴妊娠结局,促进母婴健康.

Objective To study the expression of Toll like receptor 4 (TLR4) and hepatocyte growth factor (HGF) in patients with diabetic nephropathy (DN) and its relationship with progression of DN. Methods A total of 72 cases with DN from Sep. 2014 to Sep. 2016 in our hospital were selected as DN group, then divided into high 24 h pro group (n = 31) and low 24 h pro group (n = 41) according to 24 h urinary protein quantitation (24 h pro); anther 20 healthy people in our hospital were selected as the control group. The levels of HGF and the expression of TLR4 in renal tissue were compared between the three groups. Results Compared with the control group, the expression of TLR4 in the renal tissue of DN group was significantly higher (P < 0.01), the expression of TLR4 in the renal tissue of low 24 h pro group was slightly lower than that in high 24 h pro group, but there was no significant difference between the two groups (P > 0.05). Immunohistochemical results showed that TLR4 was negative in the control group, while was overexpressed in DN group, but there was no significant difference between low 24 h pro group and high 24 h pro group (P > 0.05). Compared with the control group, the levels of HGF in serum and urine of DN group were significantly increased, and the levels of HGF in serum and urine of high 24 h pro group was significantly higher than that of low 24 h pro group, respectively; there was significant difference between the two groups (P < 0.05).Conclusion The expression of TLR4 in renal tissue of DN is closely related to the progression of DN; HGF also plays a role in the development and progression of DN.

目的 研究西维来司钠对重症急性胰腺炎(SAP)大鼠胰腺外分泌功能的影响及其作用机制.方法 将60只SD大鼠随机分为假手术组、模型组和实验组,每组20只.模型组和实验组大鼠通过向胆胰管内注入5％牛黄胆酸钠建立重症急性胰腺炎大鼠模型,假手术组仅开腹翻动十二指肠和胰腺.建模后实验组立即静脉滴注西维来司钠10 mg·kg-1,模型组和假手术组给予等量生理盐水.收集各组大鼠干预后胆胰液,并检测其中总蛋白、电解质及相关酶含量,检测各组大鼠血清生化指标水平,用苏木精-伊红(HE)染色法观察大鼠胰腺组织形态变化.结果 药物干预后24h,模型组大鼠死亡率为40.00％,实验组为10.00％,假手术组无死亡大鼠,实验组死亡率明显低于模型组(P＜0.05).实验组和模型组大鼠胆胰液中Ca2+浓度分别为(1.88±0.41),(1.02 ±0.35)mol·L-1,差异有统计学意义(P＜0.01).实验组淀粉酶(AMS)和脂肪酶(LIP)分别为(5148.21±339.58),(673.25±185.78)U·L-1,模型组分别为(7752.13±674.25),(2542.36±243.25)U·L-,差异均有统计学意义(均P＜0.01).药物干预24 h后,实验组大鼠血清中性粒细胞弹性蛋白酶(NE)、肿瘤坏死因子-α(TNF-α)、白细胞介素-2(IL-2)、白细胞介素-8(IL-8)含量均明显低于模型组(均P＜0.01).实验组胰腺病理评分为(8.52±1.04)分,明显低于模型组的(15.56±1.22)分(P＜0.01).结论 西维来司钠可降低重症急性胰腺炎大鼠死亡率,抑制胰腺分泌AMS和LIP,增加Ca2+浓度,降低中性粒细胞弹性蛋白酶及炎症因子水平,进而达到治疗重症急性胰腺炎的作用.

Objective To investigate the clinical effect and safety of interventional embolization combined with microsurgery in the hybrid operating room versus microsurgery alone in the treatment of hemorrhage from cerebral arteriovenous malformations (AVMs).Methods A retrospective analysis was performed on the clinical data of 10 patients who underwent interventional embolization combined with microsurgery in the hybrid operating room in the treatment of hemorrhage from AVMs,as well as 10 patients who underwent microsurgery alone for this disease.The two groups were compared in terms of preoperative Glasgow Coma Scale score and Spetzler and Martin grade,intraoperative blood loss,postoperative complications,and modified Rankin Scale and Glasgow Outcome Scale scores at 3 months after surgery.Results In the interventional embolization + microsurgery group,AVMs were resected completely in most cases,avoiding secondary surgery.Compared with the microsurgery group,the interventional embolization + microsurgery group had significantly less intraoperative blood loss and a significantly lower incidence of postoperative complications (both P ＜ 0.05).Conclusions For hemorrhage from AVMs,interventional embolization combined with microsurgery in the hybrid operating room is superior to microsurgery alone in terms of intraoperative blood loss,postoperative complications,and postoperative disability.

目的 观察以腹痛为主诉的糖尿病酮症酸中毒(DKA)患者血液生化特性及影像学改变特征,提高对DKA患者的误诊认识. 方法 回顾性分析本院23例以腹痛为主诉的DKA患者的血生化及影像学资料.结果 23例患者均出现不同程度的血生化改变,20例具有明显的影像学改变,18例具有明显的腹部体征.其中10例误诊为急性胰腺炎,5例误诊为急性胆囊炎,3例误诊为急性阑尾炎,2例误诊为肠梗阻,2例误诊为泌尿系结石,1例误诊为消化道穿孔.所有患者经正规补液、胰岛素降血糖、纠正酸中毒及电解质紊乱等处理后腹痛均缓解并治愈出院. 结论 以腹痛为主诉的DKA患者常出现明显的血生化及影像学改变,极易与外科腹痛相关的急腹症混淆,误诊率高,临床上应加强认识,全面问诊、系统检查,降低误诊率.